Stress-induced brain activity, brain atrophy, and clinical disability in multiple sclerosis
Stress-induced brain activity, brain atrophy, and clinical disability in multiple sclerosis
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压力引起的大脑活动、脑萎缩和多发性硬化症的临床残疾
DOI：
10.1073/pnas.1605829113
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Haynes J.D.
中科院分区：
文献类型：
--
作者：
Weygandt M;Meyer-Arndt L;Behrens J;Wakonig K;Bellmann-Strobl J;Ritter K;Scheel M;Brandt A.U;Labadie C;Hetzer S;Gold S.M;Paul F;Haynes J.D.
前瞻性临床研究支持心理应激与多发性硬化症（MS）疾病严重程度之间的联系，MS患者的外周应激系统经常失调。然而，神经生物学应激系统和MS症状之间的确切联系尚不清楚。为了评估神经应激反应和疾病参数之间的联系，我们在36名MS患者和21名健康对照者中使用了动脉自旋标记功能MRI应激范例。具体来说，我们测量了大脑活动的心算范例与性能自适应任务频率和性能反馈，并将此活动与疾病参数。在所有参与者中，与静息状态相比，压力增加了心率，感知压力以及视觉，小脑和岛叶皮层区域的神经活动。这些反应都与认知负荷（任务频率）无关。一致的是，虽然性能和认知负荷较低的患者比对照组，压力反应没有组间差异。与休息时相比，压力时胰岛素活性升高与患者锥体和大脑功能受损呈负相关。小脑激活与灰质（GM）萎缩呈负相关（即，与GM体积呈正相关）。有趣的是，在对照组的重叠区域也观察到了这种联系。认知负荷对这些关联没有贡献。结果表明，我们的任务引起的心理压力独立的认知负荷。此外，应激诱导的大脑活动反映了MS的临床残疾。最后，应激诱导的活动与患者和重叠区域对照组的GM体积之间的联系表明，这种联系不能单独由疾病引起。
Prospective clinical studies support a link between psychological stress and multiple sclerosis (MS) disease severity, and peripheral stress systems are frequently dysregulated in MS patients. However, the exact link between neurobiological stress systems and MS symptoms is unknown. To evaluate the link between neural stress responses and disease parameters, we used an arterial-spin–labeling functional MRI stress paradigm in 36 MS patients and 21 healthy controls. Specifically, we measured brain activity during a mental arithmetic paradigm with performance-adaptive task frequency and performance feedback and related this activity to disease parameters. Across all participants, stress increased heart rate, perceived stress, and neural activity in the visual, cerebellar and insular cortex areas compared with a resting condition. None of these responses was related to cognitive load (task frequency). Consistently, although performance and cognitive load were lower in patients than in controls, stress responses did not differ between groups. Insula activity elevated during stress compared with rest was negatively linked to impairment of pyramidal and cerebral functions in patients. Cerebellar activation was related negatively to gray matter (GM) atrophy (i.e., positively to GM volume) in patients. Interestingly, this link was also observed in overlapping areas in controls. Cognitive load did not contribute to these associations. The results show that our task induced psychological stress independent of cognitive load. Moreover, stress-induced brain activity reflects clinical disability in MS. Finally, the link between stress-induced activity and GM volume in patients and controls in overlapping areas suggests that this link cannot be caused by the disease alone.
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